COPD Pathogenesis & Clinical Findings PDF

Summary

This presentation details the pathogenesis and clinical findings of Chronic Obstructive Pulmonary Disease (COPD), covering genetic susceptibility, environmental factors, lung inflammation, chronic bronchitis, and emphysema. It also outlines the clinical signs of COPD, including dyspnea, wheezing, and fatigue. This resource is suitable for graduate level study or medical professionals.

Full Transcript

# COPD: Pathogenesis ## Author: Yan Yu Reviewers: Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* *MD at time of publication* ## Genetic Susceptibility - (i.e. a1-AT deficiency) ## Environmental Insult to Lungs - (i.e. long-term smoking, pollution, infection) ### Lung's ability to...

# COPD: Pathogenesis ## Author: Yan Yu Reviewers: Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* *MD at time of publication* ## Genetic Susceptibility - (i.e. a1-AT deficiency) ## Environmental Insult to Lungs - (i.e. long-term smoking, pollution, infection) ### Lung's ability to prevent damage to lung tissue: ↓ ### Free radicals produced in lungs ### Inactivation of lung anti-proteases ## Lung Inflammation - ↑ oxidative stress, inflammatory cytokines, and protease function ### Continued, repeated injury to the bronchial tree **Infiltration of inflammatory cells, esp. neutrophils** **Goblet cell proliferation, ↑ mucus production** **Death of airway epithelium ciliated cells** **↓ airway elasticity (recoil ability)** **↑ proteolytic destruction of lung parenchyma** **↓ structural supports for airway patency** **Permanent enlargement of alveoli** **Airway fibrosis and narrowing** **Mucus trapped in airways, serves as nidus for infection** **Trapping of air within lungs** **Airway narrowing and collapse** **Hyper-inflated lungs** **Bullae (easily ruptured air sacs) on lung surface** **Chronic Bronchitis** **Emphysema** # Chronic Obstructive Pulmonary Disease (COPD) ## Clinical Findings (See relevant slides) ## Complications (See relevant slides) ## Legend: - **Pathophysiology** - **Mechanism** - **Sign/Symptom/Lab Finding** - **Complications** ## COPD: Clinical Findings ### Lung Tissue Damage - If occurring around airways - ↓elastic recoil to push air out of lungs on expiration - Lungs don't fully empty, air is trapped in alveoli (lung hyperinflation) - ↑ lung volume means diaphragm is tonically contracted (flatter) ### Airflow Obstruction - ↑ mucus production - Total expiration time takes longer than normal - Prolonged expiration - Diaphragm can't flatten much further to generate deep breaths - Breathes are rapid & shallow - To breathe, chest wall must expand out more - Barrel chest - If end-stage: diaphragm will be "flat". Continued inspiratory effort further contracts diaphragm, pull the lower chest wall inwards - Hoover's sign (paradoxical shrinking of lower chest during inspiration) ### During expiration, positive pleural pressure squeezes on airways → ↑ obstruction - More effort needed to ventilate larger lungs - Respiratory muscles must work harder to breathe - Dyspnea (Shortness of breath, especially on exertion) - Turbulent airflow in narrower airways is heard on auscultation - Expiratory Wheeze - ↓ ventilation of alveoli - ↓oxygenation of blood (hypoxemia) - ↓perfusion of body tissues (i.e. brain, muscle) - Patient tries to expire against higher mouth air pressure, forcing airways to open wider - If end-stage: Chronic fatigue causes deconditioning - Fatigue; ↓ exercise tolerance - ↓ number of epithelial ciliated cells to clear away the mucus (the cells have been killed by airway inflammation) - Chronic cough with sputum - Patient breathes with accessory muscles as well as diaphragm to try to improve airflow - Pursed-lip breathing - Muscle weakness and wasting - Tripod sitting position (activates pectoral muscles) - Neck (SCM, Scalene) muscles contracted ## Legend: - **Pathophysiology** - **Mechanism** - **Sign/Symptom/Lab Finding** - **Complications**

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